Les Bio mathématiques et l'oncologie

Les Bio mathématiques et l'oncologie plateforme utile d'article et d'information sur les bio-mathématiques et les cancers de toutes ses types.

What limit can be put to this power, acting during long ages and rigidly scrutinising the whole constitution, structure,...
15/11/2018

What limit can be put to this power, acting during long ages and rigidly scrutinising the whole constitution, structure, and habits of each creature, – favouring
the good and rejecting the bad? I can see no limit to this power, in slowly and
beautifully adapting each form to the most complex relations of life.
C. Darwin, Origin of Species 1859

28/04/2018

Tout ce qui est " bio " c'est de la vie, et c'est à coup sûr, un souci à orienter en vue d'en dégager l'essence de son existence en tant que tel : l'essence de la vie, le principal élément vital, que vise le Savoir-vivre comme l' étudie " Les Bio mathématiques et l' oncologie ", cette même page où l'on le décrit.. Le bio ...la vie..

07/07/2016

La théorie de l’évolution darwinienne a récemment fêté ses 150 ans. Initialement controversée, elle occupe aujourd’hui une place centrale en biologie, expliquant l’apparition et le développement des espèces jusqu’à nos jours. Il peut être intéressant de disposer de modèles mathématiques qui rendent compte de l’évolution d’un écosystème suivant les principes darwiniens. On comprend vite que ceci est hors de portée d’un point de vue mathématique sur de grandes échelles de temps. Mais la théorie de l’évolution joue également un rôle important sur de plus petites échelles, en expliquant par exemple comment des agents microbiens (notamment les bactéries) s’adaptent à de nouvelles conditions ou encore comment des cellules tumorales réagissent à un milieu pauvre en oxygène. Dans ce cadre restreint, des modèles mathématiques peuvent être proposés et ont été effectivement développés.

Plutôt que de prendre en compte tout le génome de chaque individu, on se concentre sur un petit nombre de traits phénotypiques. Il peut s’agir de la taille à la naissance d’une bactérie ou de sa virulence par exemple. La plupart des modèles se placent dans le cadre de la reproduction asexuée et intègrent les principaux concepts de l’évolution darwinienne. Tout d’abord un individu a en général les mêmes traits que son parent : c’est l’hérédité. En revanche, dans un petit nombre de cas rares, le trait d’un descendant est différent : il s’agit de mutation. Enfin, l’ensemble des individus de la population est en compétition, directement ou pour certaines ressources, ce qui aboutit à la sélection des mieux adaptés.

A partir de ces hypothèses, on peut développer plusieurs classes de modèles, aléatoires ou déterministes. Dans le premier cas, l’évolution de chaque individu de la population est supposée aléatoire. Cependant lorsque le nombre d’individus dans la population devient trop important, on s’intéresse plutôt à la densité autour d’un trait donné. On obtient alors des modèles continus ou déterministes. Petit à petit, ces divers modèles ont été unifiés en fonction des valeurs des différents paramètres : nombre d’individus, taux et amplitude des mutations… Après de longues années d’efforts pour dépasser les difficultés théoriques, ces études mathématiques qui établissent les liens entre les différents modèles permettent de garantir que tous sont cohérents et reposent sur les mêmes bases ; en fonction de la situation, on peut ainsi librement utiliser le modèle qui semble le mieux adapté ou le plus simple à mettre en œuvre.

Brève rédigée par P.E. Jabin (University of Maryland) d’après les travaux de G. Ben Arous, N. Champagnat, L. Desvillettes, O. Diekmann, S. Méléard, S. Mirrahimi, S. Mischler, B. Perthame, G. Raoul.

The Hallmarks of cancer:in January 2000, Hanahan and Weinberg listed six alterations essential for malignant growth: sel...
26/02/2015

The Hallmarks of cancer:
in January 2000, Hanahan and Weinberg listed six alterations essential for malignant growth: self-sufficiency in growth signals, insensitivity to antigrowth signals, limitless replicative potential, ability to evade apoptosis, sustained angiogenesis, and ability to invade the tissues and metastasize, see r “The hallmarks of cancer” (Hanahan and Weinberg Cell 100:57–70, 2000)
The ability to deal with immune mechanisms, however, was not included among these essential capabilities, but may be supposed to be acquired by most—and perhaps all—tumors. Because of the authoritative impact of this paper, these six hallmarks are usually quoted as the starting ground for new anticancer strategies, while the addition of other critical features of malignant tumors as hallmarks is often urged, see ( Lazebnik Y. What are the hallmarks of cancer? Nat Rev Cancer. 2010;10:232–233. )

In the 10 years since the publication of the paper, it has become increasingly clear that both exploitation of immune mechanisms and evasion of immune surveillance are skills that cancer cells should acquire on their way to giving rise to a tumor. A comprehensive cellular, molecular, and genetic interpretation of the initially somewhat fuzzy evidence of the importance of such acquisition has also been worked out. Three such immune hallmarks are certainly required:
A) Ability to thrive in a chronically inflamed microenvironment
B) Ability to evade immune recognition
C) Ability to suppress immune reactivity

These three capabilities and acquisition of the genetic changes required to put them into practice are constant and essential features of natural and experimental cancers. Their strength, however, may vary from one kind of tumor to another, and even more variable are the mechanisms through which the various types of cancer undertake these activities. Acquisition of a specific genome change, therefore, is not important, whereas acquisition of these capabilities is crucial, irrespective of the mechanisms involved.
2011: the immune hallmarks of cancer, Cavallo et al.

21/02/2015

The biology...interresting !!

On the complexity of the biological systems:Biological systems are very different from the the physical one. ones. In fa...
19/11/2014

On the complexity of the biological systems:

Biological systems are very different from the the physical one. ones. In fact, while the latter are composed by many copies of few
elements, the former ones are constituted by a large variety of components: biological systems contain from millions to a few
copies of each of thousands of different elements, and this is one of the most important characteristic of such systems.
They are constituted by living entities which have the ability to develop a specific strategy and an organizing ability,
depending on the state of the surrounding environment. This strategy can be expressed without the application of any
external organizing principle and depends on the search of individuals for their best fitness, sometimes just for their survival.
In various cases such a skill evolves in time. In fact, living systems receive inputs from the environment and have the ability
to learn from past experience, in order to adapt themselves to the changing-in-time external conditions

Darwinian evolution: from dinosaurs to cancer drug resistance We typically think of natural selection acting on animal o...
03/08/2014

Darwinian evolution: from dinosaurs to cancer drug resistance

We typically think of natural selection acting on animal or plant species, favouring those carrying advantageous traits and making those traits more common in the next generation. However, the same process also applies to populations of cells within our own bodies. However, the same process also applies to populations of cells within our own bodies.ese mutations allow its bearer to evade cell death and reproduce more prolifically than others, it will pass that mutation on to its daughter cells, and cells bearing that mutation will expand as a clonal population within tumours and beyond.
Dr Marco Gerlinger’s work has shown that cancer isn’t a linear process of a single cell undergoing clonal expansion – it is dramatically more complex than this. In fact, the ongoing process of mutation and selection in the developing cancer creates a great diversity of cells, with many distinct genomes and behaviours. Dr Gerlinger is a team leader in the new Centre for Evolution and Cancer at The Institute of Cancer Research, London, dedicated to using Charles Darwin’s idea of evolution by natural selection to understand cancer and explore new avenues for treatment. He says: “The parallels between cancer evolution and the evolution of species are astonishing. Darwinian evolution led to the incredible diversity of species on earth. When we started to investigate diversity in human cancers at great detail, we found that the very same process also generates profound diversity in tumours.” Genetic intra-tumour heterogeneity and branched evolution, which leads to multiple different cancer sub-clones evolving in parallel within individual cancers, has since been found in a large number of solid cancer types. Treating even a single type of cancer can be a bit like trying to take aim at a whole set of moving targets all at once.
So how can we start to pin down these moving targets, which pose such a major hurdle for the development of better treatment strategies? What mutations should we be concentrating on – those found on the trunk of the evolutionary tree, or those on the branches? Dr Gerlinger says: “The ideal drug targets are probably those found on the common trunk of the evolutionary tree in an individual cancer. These genetic changes are present in every cancer cell within the tumour, and may prove more effective therapeutic targets than the heterogeneous ‘tumour branch’ events. But under specific circumstances, it may be worthwhile to target branch events. For example, patients may benefit if we can specifically attack highly aggressive sub-clones which dominate the clinical outcome, or the sub-clones which harbour mutations leading to drug resistance.” Based on these insights, one of the main aims of Dr Gerlinger’s laboratory is now to define which genes are commonly mutated on the trunk and which ones are mutated on the branches in some of the most common gastrointestinal and urological cancers.

Intra-tumour heterogeneity probably explains why resistance to cancer drugs occurs rapidly in tumours. Heterogeneous cancer cell populations within the tumour could easily include a mutant variety that happens to be resistant to any individual cancer drug we might administer.
For example, previous research has shown that when patients with colorectal cancer are treated with cetuximab – a cancer drug which is only effective in patients whose tumour does not have any KRAS mutations – mutations in KRAS can evolve over time. Research shows that KRAS mutations were already present in many tumours before treatment started but only in small numbers of cells which were not detectable. So intra-tumour heterogeneity poses a major problem for predicting drug responses. “We have to assume that resistance mutations pre-exist in many tumours but finding and quantifying them with a diagnostic test is difficult,” says Dr Gerlinger. “We’re working on highly sensitive new methods to detect such sub-clones. This may allow more precise predictions about the likelihood that an individual patient benefits from a certain treatment and to detect evolving drug-resistant clones much earlier than currently possible. Switching therapy early – before the resistant cell population has expanded dramatically and has become heterogeneous – may be beneficial by delaying the evolution of drug resistance to the next line of therapy.” A major priority of the group will be to develop biomarkers which can assess heterogeneity from a simple blood sample.

By looking at the same processes that delivered our modern day birds from dinosaurs, and drove fish from the sea to land, researchers can begin to make sense of the features of cancer which make it so difficult to conquer.

The Centre for Evolution and Cancer has been possible thanks to start-up funding from some of our philanthropic donors and from members of The Discovery Club. To donate to The Centre for Evolution and Cancer, or to become a member of The Discovery Club, please visit our Support Us pages.
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Source: ICR The Institut Cancer Rescherch 15 July 2014

Modeling Early Pancreatic Cancer (Learning About Cancer by Studying Stem Cells)Normally, when a cell becomes damaged or ...
17/07/2014

Modeling Early Pancreatic Cancer (Learning About Cancer by Studying Stem Cells)

Normally, when a cell becomes damaged or doesn't divide properly, the body's natural recycling process breaks it down and it dies. Sometimes, though, the damage is to the genes that control a cell, and the result is out-of-control division. When this happens, a cancer cell is born.

Despite decades of progress in the detection, treatment and prevention of many types of cancer, the long-term survival rate for pancreatic cancer remains very low. One reason is that pancreatic cancer rarely produces symptoms until it has spread in the body
The late stage at diagnosis also poses problems for researchers who want to study the early development of pancreatic cancer
That's because pancreatic cancer cells taken from people and then used to form tumors in animal models immediately produce the aggressive, advanced cancers from which they were derived. The lab of Kenneth Zaret of the University of Pennsylvania School of Medicine has focused on understanding how transcription factors-proteins that control which genes in a cell are expressed-work in stem cells. His team recently explored the idea of reprogramming cancer cells so they act like embryonic stem cells, which can become just about any type of cell in the body. Because transcription factors in embryonic stem cells guide early organ development, the researchers thought that forcing cancer cells back to an embryonic state might allow the transcription factors to reproduce the early stages of cancer. This could then provide a model for studying the early development of pancreatic cancer.
Using tumor tissue from people with pancreatic cancer, Zaret and his colleagues succeeded in turning a sample of cancer cells back to an early, stem cell-like state. When used to create tumors in mice, these so-called induced pluripotent stem (iPS) cells formed early stage tumors and slowly progressed to invasive disease.
The human tumors grown in mice also secreted a wide range of proteins that are indicative of cell networks known to drive pancreatic cancer progression, as well as some not previously known to be associated with the disease. "We're setting up collaborations to test these markers for their utility in screening human blood samples and see if they function as markers for detecting or predicting pancreatic cancer in humans," said Zaret.

Comment on image: Pancreatic cancer cells grown in culture. Credit: Anne Weston, London Research Institute, CRUK (image available under a Creative Commons Attribution, Non-Commercial, No Derivatives Licens
From: inside life science: of National Institute of General medical Sciences.

Mathématiques et interaction: "Théorie du chaos", en particulier pour la cancérologie.Question: En quoi consiste cette t...
14/07/2014

Mathématiques et interaction: "Théorie du chaos", en particulier pour la cancérologie.
Question: En quoi consiste cette théorie dans la mesure, c'est quoi son utilité pour la compréhension du cancer?
En 1812; Laplace a postulé que si un instant donnée la position et la vitesse de tous les objets de l’Univers étaient connues ainsi que les lois qui gouvernent leurs mouvements, on pourrait alors prédire indéfiniment aussi bien leur devenir que leur passé. Mais après, les travaux de Poincaré en 19 eme siècle ont ébranlé cette vision qui a fait de l'univers un système géant muni de loi simples (ou non) qu'il suffisait de les trouver.
L'objectif de la théorie du chaos a été spécialement développé pour appréhender les processus déterministes dont le comportement ne peut pas être prédit à long terme.
En 1963, le mathématicien Edward Lorenz, donnait des calculs visant à prouver l’impossibilité à prévoir à long terme les phénomènes météorologiques.
Dans les années 70, quelques scientifiques américains, allemands
et franc¸ ais ont commencé à s’intéresser à des systèmes
simples dont l’évolution se révélait plutôt difficile à décrire...
De là a émergé un nouveau regard sur des problèmes que nous croisons quotidiennement et qui étaient considéré pour longtemps trop complexe qui ils échappent à toute description.
Les populations animales ou cellulaires peuvent-elles
évoluer indépendamment de leur environnement, etc...
Le terme
suggestif de « chaos » a été introduit en 1975 par les deux mathématiciens Tien-Yien Li et James Yorke alors qu’ils se retrouvaient confrontés à des comportements qui leurs semblaient indescriptibles, bien qu’issus d’applications récurrentes du second degré.
Le chaos est caractérisé par une grande sensibilité aux conditions initiales: propriété très prégnante en Oncologie, pourrait également gouverner la maladie cancéreuse.
Pour une plus d'info, lire: Chaos theory: A fascinating concept for oncologists, de Denis et al.

Théorie du chaos: Fascination pour les oncologues (Les maths au cœur de l'oncologie) Resumé: papier Denisa, C. Letellier...
14/07/2014

Théorie du chaos: Fascination pour les oncologues (Les maths au cœur de l'oncologie)

Resumé: papier Denisa, C. Letellier b de FRance:
L’oncologue est quotidiennement confronté à des questions relatives au fait que pour chaque patient,
l’évolution du cancer est spécifique : il est interpellé par des évolutions très variables, inattendues et souvent
imprévisibles chez ses malades. L’approche mathématique aujourd’hui utilisée pour décrire cette
évolution est probabiliste : elle ne s’applique finalement pas à un malade spécifique, mais à une certaine
population plus ou moins hétérogène. Une telle approche caractérise donc mal la dynamique de
cette maladie et ne permet pas de dire qu’un patient est guéri, de prévoir s’il y aura rechute et quand
elle surviendra, ni de prévoir la réponse aux traitements et notamment à la radiothérapie. La théorie du
chaos, peu connue des oncologues, pourrait pourtant permettre de mieux appréhender ces questions.
Développée pour appréhender les systèmes complexes dont les comportements ne peuvent être prédits
à long terme en raison de leur grande sensibilité aux conditions initiales, la théorie du chaos est
riche de concepts propices à une nouvelle appréhension de la dynamique du cancer.

Comment:
Cette théorie est basée sur l’imprécision des éléments et la difficulté à faire des prédictions tant ces dernières peuvent être sensibles aux moindres variations

وليد يرفع التحدي في وجه السرطان باجتيازه لامتحانات الدورة الاستدراكية وليد يرفع التحدي في وجه السرطان باجتيازه لامتحانات...
09/07/2014

وليد يرفع التحدي في وجه السرطان باجتيازه لامتحانات الدورة الاستدراكية وليد يرفع التحدي في وجه السرطان باجتيازه لامتحانات الدورة الاستدراكية لنيل شهادة الباكلوريا بمصلحة أمراض الدم بمستشفى 20 غشت بالدارالبيضاء .

متمنياتنا له بالتوفيق والشفاء إن شاء الله..

De Ensemble contre le cancer

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